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Recently, a research team from Tsinghua University published a research paper titled "Intranasal prime-boost RNA vaccination elicits potent T cell response for lung cancer therapy" in the journal Signal Transduction and Targeted Therapy.
Dravet syndrome is a rare and life-changing form of epilepsy. Dravet syndrome affects approximately 1 in 15,700 children, and most cases are caused by mutations in the SCN1A gene. This gene plays a critical role in the brain's ability to regulate activity through flash interneurons. The disease has long made scientists eager to develop more effective treatments due to severe seizures and developmental delays.
Immune checkpoint inhibitor (ICI) therapy has demonstrated therapeutic benefits and prolonged survival in cancer patients. However, most patients either fail to respond to ICI therapy or develop resistance to it.
Researchers from South China University of Technology published a research paper titled "Leveraging T cell-specific fusogenicity of HIV for in vivo mRNA delivery to produce human CAR-T cells" in Cell Biomaterials, a subsidiary of Cell. The study used the T cell-specific fusion of HIV virus to develop a T cell-specific fusion virus-like particle (T-FVLP) that can mimic HIV virus and efficiently deliver CAR mRNA into T cells, thereby producing human CAR-T cells in vivo.
Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide, second only to lung cancer and gastric cancer in terms of severity. This malignant tumor originates in the liver and often occurs due to chronic hepatitis virus infection (especially hepatitis B virus). Once diagnosed, patients are often in the advanced stage of the disease. Currently, the 5-year survival rate of patients is less than 50%. In recent years, with the rise of immunotherapy, scientists have gradually realized the key role of the tumor microenvironment (TME) in cancer development, but the immune escape mechanism of HCC is still complex and not completely clear.
In a new study, researchers from the Jackson Laboratory and UConn Health not only show how cancer hijacks this tightly regulated RNA splicing and rearrangement, but also propose a potential therapeutic strategy to slow down or even shrink aggressive and hard-to-treat tumors. The discovery could change the way people treat aggressive cancers, such as triple-negative breast cancer and certain brain tumors, for which current treatment options are limited.
Stem cells are immature cells that have a fundamental regenerative role in almost all tissues. They are usually in a quiescent, slowly dividing state. But after injury, they can repair damaged tissues by switching to an activated state so that they can rapidly proliferate and become mature, functional cells. For example, hematopoietic stem cells mostly reside in the bone marrow and remain quiescent until they are stimulated or "mobilized" into the blood.
In the microscopic cellular universe, a protein called PTEN (Phosphatase and tensin homolog) is like a precise molecular brake, constantly regulating cell proliferation and survival. This "life guardian" with only 403 amino acids plays a key role in embryonic development, synaptic plasticity and even tumor suppression by antagonizing the PI3K/AKT/mTOR signaling pathway. However, surprisingly, although 30% of cancers and various neurodevelopmental diseases (such as autism and epilepsy) are closely related to PTEN dysfunction, researchers have long lacked tools to directly observe its dynamics in living tissues-until the emergence of this breakthrough study in Nature Methods ("Genetically encoded biosensor for fluorescence lifetime imaging of PTEN dynamics in the intact brain").
Promoting liver regeneration and inhibiting fibrosis is an attractive strategy for treating human liver diseases, and hepatic stellate cells (HSCs) are very important for both processes. Recently, in a research report entitled "Lhx2 specifically expressed in HSCs promotes liver regeneration and inhibits liver fibrosis" published in the international journal Hepatology, scientists from the Chinese Academy of Sciences identified the transcription factor Lhx2 (LIM homeobox protein 2) as a key regulator of hepatic stellate cells (HSCs). Lhx2 can simultaneously promote liver regeneration and inhibit liver fibrosis.
Recently, the latest research results published by researchers from the Saint Louis University School of Medicine in the journal Science Translational Medicine showed that cancer cells can produce tumor-derived extracellular vesicles (tEVs) containing PD-L1, causing PD-L1 to activate CREB and STAT signals, leading to lipid metabolism reprogramming of T cells. This induces T cell senescence and achieves immunosuppression. Blocking this process is expected to improve the sensitivity of solid tumors to immunotherapy such as PD-L1 inhibitors.
